Cancer surveys最新文献_第4页

Epstein-Barr virus infection and the pathogenesis of malignant lymphomas. eb病毒感染与恶性淋巴瘤的发病机制。

Cancer surveys Pub Date : 1997-01-01

G Niedobitek, L S Young, H Herbst

引用次数: 0

Gene therapy for B cell lymphomas. B细胞淋巴瘤的基因治疗。

Cancer surveys Pub Date : 1997-01-01

A K Fielding, S J Russell

{"title":"Gene therapy for B cell lymphomas.","authors":"A K Fielding, S J Russell","doi":"","DOIUrl":"","url":null,"abstract":"The use of genes or genetically modified cells for therapeutic benefit is likely to have a significant therapeutic role for patients with B cell lymphomas in the future. To date, most gene therapy strategies applicable to the therapy of these diseases have not reached the point of clinical study. Adoptive immunotherapy using donor leucocyte infusion to treat aggressive B cell neoplasms in immunosuppressed patients has, however, shown great promise clinically, and studies of idiotypic vaccination in patients with low grade B cell neoplasms are also under way. Results from in vitro and animal studies continue to suggest that it may become possible to use the immune system for therapeutic benefit, and many current basic research strategies in the gene therapy of B cell non-Hodgkin's lymphoma are based on immune modulation of T cells or tumour cells themselves. Other major approaches to gene therapy for B cell malignancies include the introduction of directly toxic or \"suicide genes\" into B cells or the chemoprotection of haemopoietic stem cells by the introduction of drug resistance genes. All of these approaches require efficient and accurate gene transfer as well as correct expression of the gene product within the target cell. Although some way from therapeutic use, specific targeting of gene delivery is an area of active investigation and will be of value in many of the gene therapy strategies applicable to B cell lymphomas.","PeriodicalId":77062,"journal":{"name":"Cancer surveys","volume":"30 ","pages":"327-42"},"PeriodicalIF":0.0,"publicationDate":"1997-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20471999","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Control of the G1/S transition. G1/S转换的控制。

Cancer surveys Pub Date : 1997-01-01

S I Reed

引用次数: 0

Maintaining genetic stability through TP53 mediated checkpoint control. 通过TP53介导的检查点控制维持遗传稳定性。

Cancer surveys Pub Date : 1997-01-01

G M Wahl, S P Linke, T G Paulson, L C Huang

{"title":"Maintaining genetic stability through TP53 mediated checkpoint control.","authors":"G M Wahl, S P Linke, T G Paulson, L C Huang","doi":"","DOIUrl":"","url":null,"abstract":"TP53 serves as a key relay for signals elicited by cellular stresses arising from diverse environmental or therapeutic insults. This relay then activates a cell cycle arrest or cell death program, depending on the stimulus and cell type. The absence of TP53 function disables the cell death or arrest programmes, thereby allowing the emergence of variants with various types of genomic alterations. The data discussed focus on two different types of signals that trigger the TP53 relay system. Firstly, TP53 arrests cell cycle progression in response to the types of DNA damage most commonly detected in cells undergoing tumour progression. Secondly, TP53 is activated by specific depletion of ribonucleotide pools, which prevent cells from entering S phase under conditions that could lead to chromosome breakage. The contribution of both responses limits the emergence of genetic variants. The DNA damage induced arrest appears to be triggered by as few as one double strand break in normal human fibroblasts. Analysis of the arrest kinetics after ionizing radiation shows that TP53 activates a prolonged arrest response in cells with irreparable DNA damage and that high efficiency cell elimination is achieved by a process that can be activated over multiple cell cycles. These data indicate that the primary function of the TP53 arrest/apoptosis pathway in response to double strand break is to eliminate damaged cells from the proliferating population, not to allow additional time for lesion repair. However, it remains possible that repair of other types of damage may benefit from TP53 mediated arrest. Analyses in model genetic systems indicate that the absence of TP53 function allows, but does not ensure, a high intrinsic rate of genetic variation and that instability is increased substantially when cells proceed through S phase under inappropriate growth conditions. This implies that inactivation of TP53 function in combination with other genetic alterations, such as oncogene activation, could accelerate genomic instability and tumour progression.","PeriodicalId":77062,"journal":{"name":"Cancer surveys","volume":"29 ","pages":"183-219"},"PeriodicalIF":0.0,"publicationDate":"1997-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20271394","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Genetic instability in animal tumorigenesis models. 动物肿瘤发生模型的遗传不稳定性。

Cancer surveys Pub Date : 1997-01-01

L A Donehower

引用次数: 0

Cyclin dependent kinase inhibitors. 细胞周期蛋白依赖性激酶抑制剂。

Cancer surveys Pub Date : 1997-01-01

J W Harper

引用次数: 0

Mammalian G1 and G2 phase checkpoints. 哺乳动物G1和G2期检查点。

Cancer surveys Pub Date : 1997-01-01

P M O'Connor

{"title":"Mammalian G1 and G2 phase checkpoints.","authors":"P M O'Connor","doi":"","DOIUrl":"","url":null,"abstract":"This present review explores the mechanisms for DNA damage induced G1 and G2 arrest in mammalian cells. The complexity of the TP53 pathway is attested to by the variety of genes regulated by TP53, many of which require further investigation to bring their importance into focus. One gene intensely studied, p21, has been linked to the G1 arrest mechanism and may, like TP53, be involved in some aspect of DNA repair. The outcome of TP53 activation for cell survival is equally complex and relies much upon cellular context and the type of DNA damaging agent employed. Although TP53 may participate in sensing DNA damage, additional components are likely to be required. Much of the focus on defining the mechanism of G2 arrest in mammalian cells has concentrated on the cyclin B1/CDC2 kinase. Activation of this kinase is suppressed by DNA damage, and this may result from the imposition of inhibitory phosphorylations on the CDC2 kinase as well as downregulation of cyclin B1 levels. The logical point where the G2 checkpoint interacts with the CDC2-CDC25C autocatalytic loop to prevent CDC2 activation remains to be defined and could involve inhibition of CDC25C-CDC2 interaction. It is hoped that moving upstream of CDC2 towards the point where DNA damage is sensed by the cell will uncover homologues of yeast components implicated in G2 checkpoint control. The finding that certain G2 checkpoint abrogators preferentially synergize with DNA damaging agents in cells with defective TP53 provides a potential pharmacological route through which TP53 defective cells might be targeted for destruction. Further exploration of this vulnerability might prove useful for future anti-cancer drug discovery efforts.","PeriodicalId":77062,"journal":{"name":"Cancer surveys","volume":"29 ","pages":"151-82"},"PeriodicalIF":0.0,"publicationDate":"1997-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20271515","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Molecular biology of Hodgkin's disease. 何杰金氏病的分子生物学。

Cancer surveys Pub Date : 1997-01-01

H Stein, M Hummel, T Marafioti, I Anagnostopoulos, H D Foss

{"title":"Molecular biology of Hodgkin's disease.","authors":"H Stein, M Hummel, T Marafioti, I Anagnostopoulos, H D Foss","doi":"","DOIUrl":"","url":null,"abstract":"The mist surrounding the origin and genesis of HRS cells of classical HD is beginning to dissipate. Molecular biological studies of classical HD at the single cell level strongly suggest that the HRS cells in the majority of cases represent a monoclonal outgrowth of late germinal centre B cells that have lost their capacity to express IG through crippling mutations introduced during the germinal centre reaction. Because of the expression of T cell antigens and/or cytotoxic molecules, the HRS cells of a minority of classical HD cases appear to originate from T cells. Under physiological conditions, B cells that are unable to express IG are eliminated by apoptosis. In most B cell derived classical HD cases, the HRS cells have lost their IG gene coding capacity through mutation and should therefore die of apoptosis. Since this usually does not happen, blockade of the apoptotic pathway may be a major event in the pathogenesis of B cell related classical HD. It is tempting to assume that viruses such as EBV, as well as regulator genes that normally monitor the human genome for damaged DNA, such as TP53, might be involved in the postulated hindrance of the apoptotic pathway, leading to the genesis of classical HRS cells.","PeriodicalId":77062,"journal":{"name":"Cancer surveys","volume":"30 ","pages":"107-23"},"PeriodicalIF":0.0,"publicationDate":"1997-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20469766","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Cytogenetic mechanisms in the pathogenesis and progression of follicular lymphoma. 滤泡性淋巴瘤发病和进展的细胞遗传学机制。

Cancer surveys Pub Date : 1997-01-01

T Knutsen

引用次数: 0

Primary splenic lymphoma. 原发性脾淋巴瘤。

Cancer surveys Pub Date : 1997-01-01

P G Isaacson

引用次数: 0